Myocardial subcellular glycogen distribution and sarcoplasmic reticulum Ca2+ handling: effects of ischaemia, reperfusion and ischaemic preconditioning

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Myocardial subcellular glycogen distribution and sarcoplasmic reticulum Ca2+ handling : effects of ischaemia, reperfusion and ischaemic preconditioning. / Nielsen, Joachim; Johnsen, Jacob; Pryds, Kasper; Ørtenblad, Niels; Bøtker, Hans Erik.

I: Journal of Muscle Research and Cell Motility, Bind 42, Nr. 1, 03.2021, s. 17-31.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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@article{d37ddae7cdbf494daf260dc1c0aa7d1b,
title = "Myocardial subcellular glycogen distribution and sarcoplasmic reticulum Ca2+ handling: effects of ischaemia, reperfusion and ischaemic preconditioning",
abstract = "Ischaemic preconditioning (IPC) protects against myocardial ischaemia-reperfusion injury. The metabolic and ionic effects of IPC remain to be clarified in detail. We aimed to investigate the effect of IPC (2 times 5 min ischaemia) on the subcellular distribution of glycogen and Ca2+-uptake and leakiness by the sarcoplasmic reticulum (SR) in response to ischaemia-reperfusion in cardiomyocytes of isolated perfused rat hearts (Wistar rats, 335 ± 25 g). As estimated by quantitative transmission electron microscopy, the pre-ischaemic contribution [%, mean (95% CI)] of three sub-fractions of glycogen relative to total glycogen was 50 (39:61) as subsarcolemmal, 41 (31:50) as intermyofibrillar, and 9 (5:13) as intramyofibrillar glycogen. After 25 min of ischaemia, the relative contribution (%) of subsarcolemmal glycogen decreased to 39 (32:47) in control hearts (Con) and to 38 (31:45) in IPC. After 15 min reperfusion the contribution of subsarcolemmal glycogen was restored to pre-ischaemic levels in IPC hearts, but not in Con hearts. IPC increased the left ventricular developed pressure following ischaemia-reperfusion compared with Con. In saponin-skinned cardiomyocyte bundles, ischaemia reduced the SR Ca2+-uptake rate, with no effect of IPC. However, IPC reduced a SR Ca2+-leakage at pre-ischaemia, after ischaemia and during reperfusion. In conclusion, subsarcolemmal glycogen was preferentially utilised during sustained myocardial ischaemia. IPC improved left ventricular function reflecting reduced ischaemia-reperfusion injury, mediated a re-distribution of glycogen towards a preferential storage within the subsarcolemmal space during reperfusion, and lowered SR Ca2+-leakage. Under the present conditions, we found no temporal associations between alterations in glycogen localisation and SR Ca2+ kinetics.",
keywords = "Calcium regulation, Compartmentalisation, Glycogen, Ischaemia reperfusion injury, Preconditioning",
author = "Joachim Nielsen and Jacob Johnsen and Kasper Pryds and Niels {\O}rtenblad and B{\o}tker, {Hans Erik}",
year = "2021",
month = mar,
doi = "10.1007/s10974-019-09557-3",
language = "English",
volume = "42",
pages = "17--31",
journal = "Journal of Muscle Research and Cell Motility",
issn = "0142-4319",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Myocardial subcellular glycogen distribution and sarcoplasmic reticulum Ca2+ handling

T2 - effects of ischaemia, reperfusion and ischaemic preconditioning

AU - Nielsen, Joachim

AU - Johnsen, Jacob

AU - Pryds, Kasper

AU - Ørtenblad, Niels

AU - Bøtker, Hans Erik

PY - 2021/3

Y1 - 2021/3

N2 - Ischaemic preconditioning (IPC) protects against myocardial ischaemia-reperfusion injury. The metabolic and ionic effects of IPC remain to be clarified in detail. We aimed to investigate the effect of IPC (2 times 5 min ischaemia) on the subcellular distribution of glycogen and Ca2+-uptake and leakiness by the sarcoplasmic reticulum (SR) in response to ischaemia-reperfusion in cardiomyocytes of isolated perfused rat hearts (Wistar rats, 335 ± 25 g). As estimated by quantitative transmission electron microscopy, the pre-ischaemic contribution [%, mean (95% CI)] of three sub-fractions of glycogen relative to total glycogen was 50 (39:61) as subsarcolemmal, 41 (31:50) as intermyofibrillar, and 9 (5:13) as intramyofibrillar glycogen. After 25 min of ischaemia, the relative contribution (%) of subsarcolemmal glycogen decreased to 39 (32:47) in control hearts (Con) and to 38 (31:45) in IPC. After 15 min reperfusion the contribution of subsarcolemmal glycogen was restored to pre-ischaemic levels in IPC hearts, but not in Con hearts. IPC increased the left ventricular developed pressure following ischaemia-reperfusion compared with Con. In saponin-skinned cardiomyocyte bundles, ischaemia reduced the SR Ca2+-uptake rate, with no effect of IPC. However, IPC reduced a SR Ca2+-leakage at pre-ischaemia, after ischaemia and during reperfusion. In conclusion, subsarcolemmal glycogen was preferentially utilised during sustained myocardial ischaemia. IPC improved left ventricular function reflecting reduced ischaemia-reperfusion injury, mediated a re-distribution of glycogen towards a preferential storage within the subsarcolemmal space during reperfusion, and lowered SR Ca2+-leakage. Under the present conditions, we found no temporal associations between alterations in glycogen localisation and SR Ca2+ kinetics.

AB - Ischaemic preconditioning (IPC) protects against myocardial ischaemia-reperfusion injury. The metabolic and ionic effects of IPC remain to be clarified in detail. We aimed to investigate the effect of IPC (2 times 5 min ischaemia) on the subcellular distribution of glycogen and Ca2+-uptake and leakiness by the sarcoplasmic reticulum (SR) in response to ischaemia-reperfusion in cardiomyocytes of isolated perfused rat hearts (Wistar rats, 335 ± 25 g). As estimated by quantitative transmission electron microscopy, the pre-ischaemic contribution [%, mean (95% CI)] of three sub-fractions of glycogen relative to total glycogen was 50 (39:61) as subsarcolemmal, 41 (31:50) as intermyofibrillar, and 9 (5:13) as intramyofibrillar glycogen. After 25 min of ischaemia, the relative contribution (%) of subsarcolemmal glycogen decreased to 39 (32:47) in control hearts (Con) and to 38 (31:45) in IPC. After 15 min reperfusion the contribution of subsarcolemmal glycogen was restored to pre-ischaemic levels in IPC hearts, but not in Con hearts. IPC increased the left ventricular developed pressure following ischaemia-reperfusion compared with Con. In saponin-skinned cardiomyocyte bundles, ischaemia reduced the SR Ca2+-uptake rate, with no effect of IPC. However, IPC reduced a SR Ca2+-leakage at pre-ischaemia, after ischaemia and during reperfusion. In conclusion, subsarcolemmal glycogen was preferentially utilised during sustained myocardial ischaemia. IPC improved left ventricular function reflecting reduced ischaemia-reperfusion injury, mediated a re-distribution of glycogen towards a preferential storage within the subsarcolemmal space during reperfusion, and lowered SR Ca2+-leakage. Under the present conditions, we found no temporal associations between alterations in glycogen localisation and SR Ca2+ kinetics.

KW - Calcium regulation

KW - Compartmentalisation

KW - Glycogen

KW - Ischaemia reperfusion injury

KW - Preconditioning

U2 - 10.1007/s10974-019-09557-3

DO - 10.1007/s10974-019-09557-3

M3 - Journal article

C2 - 31630282

VL - 42

SP - 17

EP - 31

JO - Journal of Muscle Research and Cell Motility

JF - Journal of Muscle Research and Cell Motility

SN - 0142-4319

IS - 1

ER -